Evidence map›Paper›PMID 39231651›Full record

ReviewEndocrine journal2025

Physiological and pathophysiological actions of insulin in the liver.

Naoto Kubota, Tetsuya Kubota, Takashi Kadowaki

Abstract readReview
In one paragraph

Review in Endocrine journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. SARS-CoV-2 Main Protease Dysregulates Hepatic Insulin Signaling and Glucose Uptake: Implications for Post-COVID-19 Diabetogenesis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Naoto KubotaDepartment of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Tetsuya KubotaDivision of Diabetes and Metabolism, The Institute of Medical Science, Asahi Life Foundation, Tokyo 103-0002, Japan.
Takashi KadowakiToranomon Hospital, Tokyo 105-8470, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver plays an important role in the control of glucose homeostasis. When insulin levels are low, such as in the fasting state, gluconeogenesis and glycogenolysis are stimulated to maintain the blood glucose levels. Conversely, in the presence of increased insulin levels, such as after a meal, synthesis of glycogen and lipid occurs to maintain the blood glucose levels within normal range. Insulin receptor signaling regulates glycogenesis, gluconeogenesis and lipogenesis through downstream pathways such as the insulin receptor substrate (IRS)-phosphoinositide 3 (PI3) kinase-Akt pathway. IRS-1 and IRS-2 are abundantly expressed in the liver and are thought to be responsible for transmitting the insulin signal from the insulin receptor to the intracellular effectors involved in the regulation of glucose and lipid homeostasis. Impaired insulin receptor signaling can cause hepatic insulin resistance and lead to type 2 diabetes. In the present study, we focus on a concept called "selective insulin resistance," which has received increasing attention recently: the frequent coexistence of hyperglycemia and hepatic steatosis in people with type 2 diabetes and obesity suggests that it is possible for the insulin signaling regulating gluconeogenesis to be impaired even while that regulating lipogenesis is preserved, suggestive of selective insulin resistance. In this review, we review the progress in research on the insulin actions and insulin signaling in the liver.

Indexed as

InsulinInsulin ResistanceLiverAnimalsDiabetes Mellitus, Type 2GluconeogenesisHumansInsulin Receptor Substrate ProteinsLipogenesisReceptor, InsulinSignal TransductionInsulinInsulin Receptor Substrate ProteinsReceptor, InsulinInsulin receptor signalingInsulin resistanceSelective insulin resistance

Identifiers

PMID39231651
PMCPMC11850106

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.